Investigation of the role of sodium chloride on wheat starch multi-structure, physicochemical and digestibility properties during X-ray irradiation.

In this paper, different NaCl content was added to wheat starch and then subjected to X-ray irradiation to investigate the effect of salt on starch modification by irradiation. The results showed that the degradation of wheat starch intensified with the increase in irradiation dose. When irradiated at the same dose, wheat starch with sodium chloride produced shorter chains, lower molecular weight and amylose content, and higher crystallinity, solubility, and resistant starch than wheat starch without sodium chloride. The energy generated by X-rays dissociating sodium chloride caused damage to the glycoside bonds of the starch molecule. With a further increase in the mass fraction of NaCl, the hydrogen bonds of the starch molecules were broken, and the double helix structure was depolymerized, which exacerbated the extent of irradiation-modified wheat starch. At the same time, starch molecules will be rearranged to form a more stable structure.

The complete chloroplast genome of Ficus pumila, a functional plant in East Asia.

Ficus pumila L. is a climbing fig commonly used as an ornamental plant. In this study, we sequenced and assembled the complete chloroplast genome of F. pumila. The complete chloroplast genome of F. pumila is 160,248 bp in length which includes a pair of inverted repeats (IRs) of 25,871 bp separated by a large single-copy (LSC) region of 88,405 bp and a small single-copy (SSC) region of 20,101 bp. The overall guanine-cytosine (GC) content of F. pumila cp genome is 35.98%, while the corresponding values of LSC, SSC, and IR sequences are 33.65, 29.05, and 42.65%, respectively. The phylogenetic tree was shown to be consistent with the traditional morphology-based taxonomy of Moraceae. Five plants from the genus Ficus formed a well-supported monophyletic clade with 100% bootstrap value, and F. pumila is closely related to F. hirta, F. carica, and F. racemosa, with a support value of 97%. The complete chloroplast of F. pumila contributes to the growing number of chloroplast genomes for phylogenetic and evolutionary studies in Moraceae.

Endogenous H2O2-Sensitive and Weak Acidic pH-Triggered Nitrogen-Doped Graphene Nanoparticles (N-GNMs) in the Tumor Microenvironment Serve as Peroxidase-Mimicking Nanozymes for Tumor-Specific Treatment.

Nanozymes are emerging as a promising strategy for the treatment of tumors. Herein, to cope with the tumor microenvironment (TME), weak acidity (pH 5.6 to 6.8) and trace amounts of overexpressed hydrogen peroxide (H2O2) (100 µM-1 mM), we report nitrogen-doped graphene nanomaterials (N-GNMs), which act as highly efficient catalytic peroxidase (POD)-mimicking nanozymes in the TME for tumor-specific treatment. N-GNMs exhibit POD catalytic properties triggered by a weakly acidic TME and convert H2O2 into highly toxic hydroxyl radicals (•OH) thus causing the death of tumor cells while in the neutral pH surroundings of normal tissues, such catalysis is restrained and leaves normal cells undamaged thereby achieving a tumor-specific treatment. N-GNMs also display a high catalytic activity and can respond to the trace endogenous H2O2 in the TME resulting in a high efficiency of tumor therapy. Our in vitro chemical and cell experiments illustrated the POD-like activity of N-GNMs and in vivo tumor model experiments confirmed the significant inhibitory effect of N-GNMs on tumor growth.

A barrier against reactive oxygen species: chitosan/acellular dermal matrix scaffold enhances stem cell retention and improves cutaneous wound healing.

BACKGROUND: Stem cell therapies have gained great attention for providing novel solutions for treatment of various injuries and diseases due to stem cells' self-renewal, ability to differentiate into various cell types, and favorite paracrine function. Nevertheless, the low retention of transplanted stem cell still limits their clinical applications such as in wound healing in view of an induced harsh microenvironment rich in reactive oxygen species (ROS) during inflammatory reactions. METHODS: Herein, a novel chitosan/acellular dermal matrix (CHS/ADM) stem cell delivery system is developed, which is of great ROS scavenging activity and significantly attenuates inflammatory response. RESULT: Under ROS microenvironment, this stem cell delivery system acts as a barrier, effectively scavenging an amount of ROS and protecting mesenchymal stem cells (MSCs) from the oxidative stress. It notably regulates intracellular ROS level in MSCs and reduces ROS-induced cellular death. Most importantly, such MSCs delivery system significantly enhances in vivo transplanted stem cell retention, promotes the vessel growth, and accelerates wound healing. CONCLUSIONS: This novel delivery system, which overcomes the limitations of conventional plain collagen-based delivery system in lacking of ROS-environmental responsive mechanisms, demonstrates a great potential use in stem cell therapies in wound healing.

SIRT1/PGC-1 pathway activation triggers autophagy/mitophagy and attenuates oxidative damage in intestinal epithelial cells.

Oxidative stress leads to intestinal epithelial cells damage, which induces tight junction injury and systemic endogenous stress syndrome. The evidence suggests that SIRT1/PGC-1α pathway is closely associated with oxidative damage. However, the mechanism in protecting intestinal epithelial cells against oxidative stress dependant on autopahgy/mitophagy remains to be elucidated. In the current study, we investigated the functional role of SIRT1/PGC-1α pathway on regulation of autopahgy/mitophagy and tight junction protein expression underlying the oxidative dysfunction in porcine intestinal epithelial cells (IPEC-1). Results demonstrated that H2O2 exposure caused high accumulation of ROS, with a decrease of mitochondrial membrane potential and an inhibition of the tight junction molecules in IPEC-1 cells. Also, COX IV mRNA expression and SIRT1/PGC-1α pathway were suppressed. Autophagy and PINK1/Parkin dependant-mitophagy were activated following H2O2 treatment. Further research indicated that activation of SIRT1/PGC-1α pathway caused by specific activator SRT 1720 resulted in elevating autophagy/mitophagy related markers and SIRT1 inhibitor EX 527 reversed these effects. Additionally, SIRT1 activation significantly suppressed the ROS generation, leading to increase mitochondrial membrane potential and COX IV expression. Most importantly, the expression of tight junction molecules contributing to maintain intestinal barrier integrity was significantly up-regulated. Collectively, these findings indicated that autophagy/mitophagy elevation caused by SIRT1/PGC-1α pathway activation might be a protective mechanism to increase tight junction integrity against oxidative stress-mediated ROS production in IPEC-1 cells.

Acidic pH and High-H2O2 Dual Tumor Microenvironment-Responsive Nanocatalytic Graphene Oxide for Cancer Selective Therapy and Recognition.

It is well known that tumors have an acidic pH microenvironment and contain a high content of hydrogen peroxide (H2O2). These features of the tumor microenvironment may provide physiochemical conditions that are suitable for selective tumor therapy and recognition. Here, for the first time, we demonstrate that a type of graphene oxide nanoparticle (N-GO) can exhibit peroxidase-like activities (i.e., can increase the levels of reactive oxygen species (ROS)) under acidic conditions and catalyze the conversion of H2O2 to ROS-hydroxyl radicals (HO·) in the acidic microenvironment in Hela tumors. The concentrated and highly toxic HO· can then trigger necrosis of tumor cells. In the microenvironment of normal tissues, which has a neutral pH and low levels of H2O2, N-GOs exhibit catalase-like activity (scavenge ROS) that splits H2O2 into O2 and water (H2O), leaving normal cells unharmed. In the recognition of tumors, an inherent redox characteristic of dopamine is that it oxidizes to form dopamine-quinine under neutral (pH 7.4) conditions, quenching the fluorescence of N-GOs; however, this characteristic has no effect on the fluorescence of N-GOs in an acidic (pH 6.0) medium. This pH-controlled response provides an active targeting strategy for the diagnostic recognition of tumor cells. Our current work demonstrates that nanocatalytic N-GOs in an acidic and high-H2O2 tumor microenvironment can provide novel benefits that can reduce drug resistance, minimize side effects on normal tissues, improve antitumor efficacy, and offer good biocompatibility for tumor selective therapeutics and specific recognition.

Knockdown of long noncoding RNA urothelial carcinoma associated 1 inhibits colorectal cancer cell proliferation and promotes apoptosis via modulating autophagy.

Long noncoding RNA urothelial carcinoma associated 1 (UCA1) has been implicated in the growth and metastasis of colorectal cancer (CRC), and autophagy contributes to tumorigenesis and cancer cell survival. However, the regulatory role of UCA1 in CRC cell viability by modulating autophagy remains unclear. In the present study, a significant positive correlation was observed between UCA1 and microtubule-associated protein 1 light chain 3 (LC3) levels, and the elevated UCA1 was negatively correlated with the PKB/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway in 293T cells. Downregulation of UCA1 inhibited autophagy activation and cell proliferation, whereas the apoptosis was increased and the cell cycle was arrested in G2 stage. The next results showed that UCA1 was markedly upregulated in Caco-2 cells. Knockdown of UCA1 significantly decreased the LC3-II and autophagy-related gene 5 (ATG5) protein levels and resulted in an increase in p62 expression. Conversely, the autophagy activator rapamycin (RAPA) reversed the effects. Furthermore, downregulated UCA1 decreased Caco-2 cells population in the G1 phase and increased the cells number in G2 phage. The cell proliferation was inhibited, and apoptosis rate was promoted. More important, RAPA could also abrogate the changes induced by knockdown of UCA1. Collectively, these data demonstrated that downregulated UCA1 induced autophagy inhibition, resulting in suppressing cell proliferation and promoting apoptosis, which suggested that UCA1 might serve as a potential new oncogene to regulate CRC cells viability by modulating autophagy.

Preparation of Lanthanide Ions-Doped BiPO4 Nanoparticles and Fe3+ Ions Assay.

A facile method for the synthesis of a Ln3+ (Eu, Tb) doped BiPO4 (BPO) nanocrystals were developed using an environment-friendly low temperature hydrothermal method assisting with phenol formaldehyde resin (PFr). Structure and surface functional groups of BPO samples were characterized by XRD and IR patterns. Morphology was studied by SEM technology also. Furthermore, doped BPO display strong red and green emissions from Eu3+ and Tb3+ ions respectively, and the BPO suspension is selectively quenched upon addition Fe3+ ions, and there is barely any interference by other metal ions, thus making the nanocrystals as a potential Fe3+ ions Fluorescent Probe, and the detection limit is below micromole level.

MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50).

Inflammation is the body's normal self-protection mechanism to eliminate pathogens and resist pathogen invasion. The excessive inflammatory response may lead to inflammatory lesions. The mechanisms accounting for inflammation remain hazy. miRNAs have been proposed to have crucial effects on inflammation. In the present study, we reported that lipopolysaccharide (LPS)-stimulation increased the expression levels of inflammatory cytokines and the cell-cycle progression was suppressed in RAW264.7 cells. Meanwhile, the expression of miR-322 was significantly down-regulated after LPS treatment. Bioinformatics predictions revealed a potential binding site of miR-322 in 3'-UTR of NF-κB1 (p50) and it was further confirmed by luciferase assay. Moreover, both the mRNA and protein levels of NF-κB1 (p50) were down-regulated by miR-322 in RAW264.7 cells. Subsequently, we demonstrated that miR-322 mimics decrease in the expression levels of inflammatory cytokines and cell-cycle repression can be rescued following LPS treatment in RAW264.7 cells. The anti-inflammatory cytokines expression including IL-4 and IL-10 were significantly up-regulated. Furthermore, miR-322 could also promote RAW264.7 cells proliferation. These results demonstrate that miR-322 is a negative regulator of inflammatory response by targeting NF-κB1 (p50).